ArticleNature communications2019
Impaired cellular energy metabolism in cord blood macrophages contributes to abortive response toward inflammatory threats.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 60 citations in OpenAlex.
- Maturation-Dependent Constraints in the Ability of Human Monocytes to Initiate Trained Immunity.MedComm · 2026Article
- Neonatal monocyte iron metabolism and immunometabolic responses in sepsis: a comparative ex vivo investigation.Pediatric research · 2026Article
- Circular RNA circIGF1R controls cardiac fibroblast proliferation through regulation of carbohydrate metabolism.Scientific reports · 2025Article
- Oxidative phosphorylation is a key feature of neonatal monocyte immunometabolism promoting myeloid differentiation after birth.Nature communications · 2025Article
- Article
- A Self-Assembled Metabolic Regulator Reprograms Macrophages to Combat Cytokine Storm and Boost Sepsis Immunotherapy.Research (Washington, D.C.) · 2025Article
- Seminal plasma S100A8/A9 as a potential biomarker of genital tract inflammation.Asian journal of andrology · 2024Article
- Targeting Macrophage Polarization for Reinstating Homeostasis following Tissue Damage.International journal of molecular sciences · 2024Review
- Article
- New Insights in Immunometabolism in Neonatal Monocytes and Macrophages in Health and Disease.International journal of molecular sciences · 2023Review
- BCG-Induced Immune Training: Interplay between Trained Immunity and Emergency Granulopoiesis.Journal of molecular biology · 2023Review
- Decreased expression of hypoxia-inducible factor 1α (HIF-1α) in cord blood monocytes under anoxia.Pediatric research · 2023Article
- 1,2-Current issues in molecular biology · 2023Article
- Identification of an Immune-Related Gene Diagnostic Model and Potential Drugs in Sepsis Using Bioinformatics and Pharmacogenomics Approaches.Infection and drug resistance · 2023Article
- Monocyte signature as a predictor of chronic lung disease in the preterm infant.Frontiers in immunology · 2023Article
- Glucose supply and glycolysis inhibition shape the clinical fate of Staphylococcus epidermidis-infected preterm newborns.JCI insight · 2022Article
- Neuroprotective Effects of Celastrol in Neurodegenerative Diseases-Unscramble Its Major Mechanisms of Action and Targets.Aging and disease · 2022Review
- Celastrol mitigates inflammation in sepsis by inhibiting the PKM2-dependent Warburg effect.Military Medical Research · 2022Article
- Can polarization of macrophage metabolism enhance cardiac regeneration?Journal of molecular and cellular cardiology · 2021Article
- The Distinct Immune Nature of the Fetal Inflammatory Response Syndrome Type I and Type II.ImmunoHorizons · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neonatal sepsis is characterized by hyperinflammation causing enhanced morbidity and mortality compared to adults. This suggests differences in the response towards invading threats. Here we investigate activated cord blood macrophages (CBMΦ) in comparison to adult macrophages (PBMΦ), indicating incomplete interferon gamma (IFN-γ) and interleukin 10 (IL-10)-induced activation of CBMΦ. CBMΦ show reduced expression of phagocytosis receptors and cytokine expression in addition to altered energy metabolism. In particular, IFN-γ as well as IL-10-activated CBMΦ completely fail to increase glycolysis and furthermore show reduced activation of the mTOR pathway, which is important for survival in sepsis. MTOR inhibition by rapamycin equalizes cytokine production in CBMΦ and PBMΦ. Finally, incubation of PBMΦ with cord blood serum or S100A8/A9, which is highly expressed in neonates, suppresses mTOR activation, prevents glycolysis and the expression of an PBMΦ phenotype. Thus, a metabolic alteration is apparent in CBMΦ, which might be dependent on S100A8/A9 expression.
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